川崎病如今已是儿童后天性心脏病的最常见病因之一，可导致严重致死性心血管并发症，尤以冠状动脉瘤带来的后果最为严重。因此，探索冠状动脉瘤的形成机制在川崎病的治疗过程中占据重要地位，但当前，有关动脉瘤形成机制的研究尚且不足。本课题组在前期研究中发现：骨桥蛋白（OPN）的表达量较高的血管中，血管壁炎症浸润较多，而血管壁胶原蛋白的含量却较低；反之，OPN表达量较低的血管中，血管壁的炎症浸润较少，而胶原蛋白的含量较高。而炎症的浸润、胶原蛋白的减少，会造成血管壁的变薄和不完整，并进而在血流的作用下形成动脉瘤，由此推测，OPN可能在促进动脉瘤形成过程中起到重要作用。本课题拟从动物、细胞水平明确OPN在动脉瘤形成过程中的重要作用和相关分子机制，进而借助分子影像技术验证OPN作为分子靶点对动脉瘤的诊断，以期为川崎病动脉瘤形成提供新的诊疗手段和治疗分子靶点。

Kawasaki disease has become one of the leading causes of acquired cardiac disease in children, which can result in devastating cardiovascular complications. Among cardiovascular complications, coronary artery lesions in particular can lead to long term morbidity and mortality, especially the development of coronary artery aneurysm. Although it carries great clinical importance and necessity to explore the mechanisms underlying aneurysm formation, researches related to this topic are far from enough. Since our former researches revealed that artery which got more macrophages’ infiltration and less collagen expressed higher OPN, and serious inflammation and degraded collagen always led to incomplete and tunica artery wall where aneurysm formed easily, we assumed OPN could be a key target to prevent the aneurysm from formation. Our project was designed to assess the role of OPN in aneurysm formation and the underlying mechanisms. Then animal models were built to evaluate efficacy of OPN-targeted nanoprobes to monitor aneurysm lesions via molecular imaging in vivo. This project aims to provide a new target for KD’s warning diagnosis and on-time treatment.